It has been commonly assumed that estrogen plays at least some role in the retention of body fat in males, particularly when attempting to lean out severely (i.e., contest prep). Indeed, Mr. Don Alessi has made the claim that by assessing one’s fat retentive areas one can determine if their fat profile is more associated with estrogenic fat or insulin resistence. For quite some time, fat topography, and more specifically adipose tissue endocrinology has been a pursuit of mine to determine just how much and to what extent certain areas of fat on the body are related to various endocrinological nuances or disturbances.
As such, I wanted to throw out what appears to be the latest reserach on estrogen and fat, and see if anecdotally, there are different reports.
Estrogenic fat areas are commonly assummed (perhaps incorrectly) to be such areas as behind the tricep, around the lower back, and around the navel (in males). In addition, it is well known that gynecomastia is directly estrogen related. This common assumption has lead to the use of anti-e’s and anti-aromatase formulas following cycles and during diet phases to allow for the prevention or reduction of what is believed to be estrogenic fat.
Ken Stark was the first to point out a study that seemingly showed that treatment of male-female transexuals with estradiol resuled in increased subcutaneous fat on the original male subjects (Elbers et al., 1999). However, a recent comprehensive review of the role of estrogen and estrogen receptor alpha in male adipose tissue (Cooke et al., 2001) suggests that estrogen is higly implicated in regulating white adipose tissue in male, and that males who lack both ER alpha and beta receptors show increased fat gain/retention. They further postulate that since this is not due to hyperphagia (the fat gain) that estrogen acts on the male body in a myriad of ways, primary amongst which one is controlling basal metabolis rate. They also offer the following seemingly surprising points:
1)…"Although both human and animal studies suggest estrogen may affect glucose tolerance and insulin resistance in females by direct actions on adipocytes to increase insulin receptor expression (references)…Estrogen also appears to act on WAT (White Adipose Tissue) through alteration of leptin production and hypothalamic leptin expression
2)…"The altered glucose tolerance and insulin resistance in the ERalpha knockout mice could be a major factor in the etiology of the increased WAT in both sexes. The insulin resistance and impaired glucose tolerance, as well as the increase in male WAT, in mice lacking ERalpha was similar to those reported for the aromatase knockout mouse and the insulin resistance and glucose tolerance findings in alpha ERKO and ArKO mice parallel observations in humans lacking ERalpha or aromatase.
3)**"There has been intense recent interest in the potential benefits of phytoestrogens, estrogenic compounds found in soybeans and other plants. These compounds may also be beneficial in regulating WAT in humans…The primary phytogestrogen in soy is the isoflavone genisten…genisten and some other isoflavones act as weak estrogens…could the ability of genisten and other phytoestrogens to signal through ERalpha be one contributor to the lower obesity levels seen in populations that consume higher amounts of these compounds? Nogowski et al. (1988) have shown that genisten can act on adipocytes to strongly depress both their basal and insulin-induced lipid synthesis and that genisten can have effects on triglyceride and free fatty acid concentrations in the serum.
Returning to the original study pointed out by K. Stark, the male-female transexuals were treated with both estradiol and an anti-androgen. Perhaps it was the anti-androgen, not the estradiol that allowed for the increase in subcutaneous body fat. After all, T is a major regulator of subcutaneous body fat, and its reduction would most likely act to increase the turnover of that particular type of fat. Furthermore, it has been demonstrated that animals treated with estrogens such as estradiol or the synthetic estrogen zeranol have both decreased fat and incrased lean muscle mass.
In conclusion, I might state that I continue to be confused by the role of E in what may be subcutaneous body fat retention and patterning in males. Perhaps there is none, although anecdotal reports of cycles of clomid and other anti aromatases and estrogens indicate that they greatly reduce fat, particularly around the umbilical region. Then again, this may be due to the fact that renal sensitivity to AVP may be lower during E due to intrarenal effects on water and sodium as estrogen/progesterone treatment has been shown to increase sodium retention and renin-angiotensin-aldosterone stimulation.
Vain
